1. Field of the Invention
The present invention is directed generally to medical procedures and, more particularly to a medical procedure for removal of the innermost layer of the human retina (internal limiting membrane) from the underlying neural retina at the center of vision (macula).
2. Background Art
The rays of light entering the eye (FIG. 1) and bearing the pattern of the object being looked upon pass through the cornea 32, the aqueous humor, the pupil, the lens 34, and the vitreous humor, then fall upon the retina 26. The retina is the light sensitive film lining the back two-thirds of the eye. Its appearance is similar to that of wet tissue paper. Its layers consist of the internal limiting membrane (ILM), the neurosensory retina, and the retinal pigment epithelium; the ILM, being innermost, is the retinal border with the vitreous gel cavity 42. If the parts of the eye are normal and the lens is properly adjusted, the image will be focused upon the retina. This condition results in clear vision. At the back of the eye or, more specifically, the back part of the retina is the macula lutea 36 having at its center the fovea centralis. The macula is a small orange-yellow, oval area (about 3 mm by 5 mm) of the retina adjacent to the optic nerve 38. Vision in which the image of the object looked upon falls upon the macula is the sharpest vision and is called macular vision or central vision, as opposed to gross, peripheral vision.
A wrinkling of the internal limiting membrane and the neural retina is called macular pucker. This can cause loss of fine vision to the level of legal blindness. The wrinkling is caused by contractile cells or fibrocellular membranes (epimacular proliferation or EMP) and is usually a process associated with aging.
Macular distortion and macular edema, with resultant macular dysfunction, are recognized sequelae of EMP. Often, the macula will have a "wrinkled cellophane" appearance. According to one theory, this appearance represents internal limiting membrane (ILM) distortion by surface proliferative cells without a distinct epimacular proliferative membrane overlying the ILM, which might be surgically removed. This ILM cellophaning may persist or occur months after seemingly successful removal of EMP, limiting visual recovery.
Specimens analyzed after vitrectomy (the surgical removal of a portion of the vitreous body and/or associated epiretinal or fibrous membranes) using a microscope for epimacular membrane removal often contain retinal ILM fragments that have been intentionally or unintentionally removed to treat "traction maculopathy," a term introduced by Morris, R., Kuhn, F., Witherspoon, C. D., ("Retinal folds and hemorrhagic macular cysts in Terson's syndrome," Ophthalmology (1994) 101:1). Written reports differ on whether the presence of ILM fragments correlate with the visual outcome. (Trese, M. et al., "Macular pucker Ultrastructure," Graefe's Arch Clin Exp Ophthamol. (1983)221:16-26; De Bustros, S. et al., "Vitrectomy for Macular Pucker: Use after treatment of retinal tears or retinal detachment," Arch Ophthalmol. (1988) 106:758-760; Sivalingam, A. et al., "Visual prognosis correlated with the presence of internal limiting membrane in histophathologic specimens obtained from epiretinal membrane surgery," Ophthalmology. (1990) 97:1549-1552). More recently, William Hutton and others have implicated even relatively small amounts of traction as exacerbating diabetic macular edema.
Additionally, Logan Brooks and Tom Rice have advocated the intentional removal of the macular ILM in macular hole surgery. (Brooks, L., "ILM peeling in full thickness macular hole surgery," Vitreoretinal Surgery and Technology. (1995) 7:2; Rice, T. A., "Technique of removal of the inner retinal surface in macular hole surgery," Retina Society 28.sup.th Annual Meeting. Santa Fe, N.Mex., 1995). A macular hole is thought to occur as a result of tangential traction on the retina at the macula, usually leading to legal blindness
Thus, there are many advocates of the importance of ILM removal in macular hole surgery. Previous methods as shown in FIG. 2, developed over a period of about twenty years, have removed the macular ILM 54 and EMP 50 utilizing the manual, mechanical method with grasping forceps 52. This forceps procedure is the most delicate surgical maneuver performed on the human body. The procedure requires ideal surgical conditions and expert skill. Ideally, cataracts and any other opacity obscuring surgical view will have been eliminated for safe and predictable EMP/ILM removal. Electron microscopy of surgical specimens frequently demonstrates cellular proliferation contracting the ILM. It is believed that the increased mobility of an ILM denuded macula contributes to successful hole closure.
Furthermore, the results with ILM maculorhexis in macular hole surgery were encouraging. In a consecutive series of 32 idiopathic holes with less than two years duration, a 97% closure was achieved. Previous macular hole edges were rarely discernible. Visual acuity improved at least two Snellen lines in 91% of eyes, and 41% of eyes achieved 20/40 or better visual acuity at the last follow-up (Morris, R., Witherspoon, C. D., "Internal Limiting Membrane Maculorhexis for Traction Maculopathy," Vitreoretinal Surgery and Technology (1997) 8(4):1).
All of the above-described conditions may be considered forms of traction maculopathy as first described by Morris et al. The ultimate goal of all surgery to cure traction maculopathy is to return the neural retina to its normally smooth contour, allowing resumption of fine vision and relief from distorted vision.
In a very rare disease called Terson's syndrome, blood under pressure from a ruptured vein or capillary spontaneously lifts the ILM, resulting in what is called a hemorrhagic macular cyst (HMC) (Morris, R., Kuhn, F., Witherspoon, C. D., American Academy of Opthalmology, 1990). The hemorrhage usually then breaks through the ILM into the vitreous. Vitreous and subinternal limiting membrane hemorrhage occurs as a result of abrupt intracranial hemorrhage from an aneurysm or closed head trauma. Although the exact mechanism for these hemorrhages is unknown, it is thought that the sudden increased intracranial pressure is transmitted via the optic nerve to retinal venules and capillaries, rupturing them. If bleeding has occurred at the macula, it will appear as a circular or boat shaped cyst (HMC) on the surface of the retina. The HMC is usually encircling the macula. Its diameter and height vary, as does its color, depending on the longevity of the hemorrhage. Early intervention (i.e., for amblyopia prevention in infants) finds a reddish cyst. A few months after the incident, the surgeon encounters a yellow lesion (degenerated blood products), a clear membrane spanning an optically empty cavity, or a collapsed membrane. A perimacular fold may form along the edge of the separation of the ILM from the neurosensory retina at the cyst margin.
Sub ILM hemorrhagic macular cysts are almost pathognomic to Terson's syndrome. Fourteen cases of retinal folds from shaken baby syndrome or consequent to direct head trauma were analyzed from various literature reports, each had intracranial hemorrhage and various forms of intraocular hemorrhage, including HMC. The HMC's occur not only in traumatically induced cases of Terson's syndrome but also in patients with spontaneous subarachnoid hemorrhage. Accordingly, it has been proposed that intracranial hemorrhage, from whatever source, is the common denominator in the formation of both HMC's and their accompanying perimacular folds.
In the series originally presented at the Annual Meeting of the American Academy of Ophthalmology in 1990, it was found that of 25 eyes undergoing vitrectomy for Terson's syndrome, 8 (32%) demonstrated HMC's (Morris, R., Kuhn, F., Witherspoon, C. D., "Hemorrhagic Macular Cysts in Terson's Syndrome and its Implications for Macular Surgery," Developments in Opthalmology (1997) 29:44). After careful clinical examinations and light or electron microscopic evaluations, it was concluded that the ILM had formed the anterior cyst wall in five eyes. While several literature reports have characterized these hemorrhagic lesions as being subvitreous or under a proliferative membrane, it is believed by Morris et al. (see above) that the majority of hemorrhagic macular cysts in Terson's syndrome are in fact submembranous (beneath the ILM) rather than subvitreous (preretinal).
Although rare, submembranous HMC's in Terson's syndrome are the most frequent lesion in which the macular ILM is spontaneously lifted from the underlying neurosensory retina as a result of a disease process. Thus, it was postulated that if the denuded macula retains good function without reparative surface proliferation developing, similar non-traumatic surgical removal of the ILM during vitrectomy in certain cases of traction maculopathy might be endorsed. (Morris, R., Kuhn, F., Witherspoon, C. D., "Retinal folds and hemorrhagic macular cysts in Terson's syndrome," Ophthalmology (1994) 101:1). For example, in none of the five Terson's eyes in a series evaluated by the inventor and colleagues did reparative proliferation develop during an average follow up of 32 months (range: 6-70 months), and all adult eyes reached and maintained excellent 20/25 visual acuity.
Therefore, the desirability of developing procedures for the atraumatic surgical removal of the macular ILM in certain forms of traction maculopathy was suggested. ("Hemorrhagic Macular Cysts in Terson's Syndrome and its Implications for Macular Surgery," Developments in Ophthalmology (1997) 29:44). Even minimal ILM surface traction has been increasingly implicated in many forms of maculopathy and often the EMP/ILM layers become, in effect, fused together, not allowing surgical removal of EMP alone. Additionally, long-term macular function appears to be stable or improved even without the ILM. ("Hemorrhagic Macular Cysts in Terson's Syndrome and its Implications for Macular Surgery," Developments in Ophthalmology (1997) 29:44). Thus, ILM removal is an important technique in the treatment of all forms of traction maculopathy because only the removal of the ILM with all cellular and membrane proliferation on its surface ensures total relief from all traction on the underlying nerve fibers at the center of vision. However, the methods thus far developed for such ILM removal have certain deficiencies. The method of mechanical pulling tearing away the macular ILM with forceps can cause severe trauma to the macula and the resultant injury can cause ocular damage of equal severity to the problem the surgery is meant to correct.
The current method employed for removal of both EMP and the macular ILM consists of cutting and then grasping, or directly grasping, the macular EMP/ILM with specially designed micro-forceps, 1 mm in maximum diameter, and slowly pulling it apart from the neural retina. This is done with great care in order to avoid engaging the neurosensory retina.
One problem with the current method of tearing and peeling away the macular ILM is the physical trauma associated with pulling on the ILM until it separates thereby unavoidably stressing the underlying nerve tissue, sometimes causing irreparable nerve damage with worsened vision than may have been present preoperatively. Accordingly, the surgeon may proceed slowly and carefully but if too slowly the retina may be injured from light toxicity coming from the fiberoptic probe inside the eyeball enabling the surgeon's view. If the surgeon grasps too shallow then his movements are ineffectual, adding to the time of surgery and the chance of light toxicity. If the surgeon grasps too deep, permanent nerve damage and hemorrhage results. The difference is usually a matter of microns of forceps movement, causing the surgeon's mindset to be what has justly been described as "nerve-wracking." The mass of the forceps, although ever so small, often obscures the surgeon's view, further adding to the chance of surgical damage to the retina. As a result of the above factors, complete traction release is the exception rather than the rule. Finally, even in the unusual case of complete traction release, the nerve tissue will usually require several months to resume a smooth contour with best vision returning. Thus, for some twenty years, the removal of epimacular proliferation so as to restore central vision in the eyes that are approaching legal blindness has remained a vexing problem for vitreoretinal surgeons worldwide. The potential surgical risks and the uncertain benefits, as well as the high level of skill required to perform such surgery has caused many surgeons to be reluctant to intervene until vision is substantially lost. This has been true, despite the knowledge that persistence of EMP causes permanent destruction of nerve function at the center of vision, such that visual acuity is only partially restorable, and progressively less so, as the EMP is allowed to persist.
Solutions have been diligently sought over this twenty-year period, including progressively smaller and finer forceps. Finally, as an illustration of surgeons' frustration, in 1997, a new concept was introduced by Tano to surgically rub or scrape the surface of the retina at or near the macula with a flexible, rubber instrument upon which has been glued innumerable diamond chips so as to allow the device to purchase a hold on these barely visible membranes and/or ILM. This device was introduced and has been substantially used, despite the obvious risk of damage to the neural retina which underlays these thin membranes by rubbing or scraping the retinal surface with an intentionally roughened instrument, as well as the risk of diamond chips dislodging and permanently remaining on the retinal surface within the eye. These risks have been tolerated in the more or less desperate search for effective remedies for traction maculopathy because the device adds an additional means to gain a surgical edge against the all too frequent need to conclude the operation before achieving complete release of traction.
Wang U.S. Pat. No. 5,066,276, described injecting viscous material into the eye using a standard glue injector. Wang, however, did not apply this surgical procedure within the retina itself. Rather, Wang described injecting the viscous material between a glia cell membrane and the retina. Wang described his procedure as one in which the pressure applied to the retina is very diffuse and not localized in one small area in order to reduce stresses on the retina.
There remains a need for improved methods for removal of both epimacular proliferations and the abnormal ILM of the retina to completely relieve all forms of traction maculopathy in which the ILM is contributory. Such a method must be based upon minimizing surgical traction on the underlying nerve tissue at the center of vision (fovea). The method and apparatus described herein overcomes the above noted problems.